A Missing Link Between a High Salt Intake and Blood Pressure Increase
Abstract.: It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them pro...
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| Format: | Article |
| Language: | English |
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Elsevier
2006-01-01
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| Series: | Journal of Pharmacological Sciences |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1347861319344858 |
| _version_ | 1819112387518660608 |
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| author | Makoto Katori Masataka Majima |
| author_facet | Makoto Katori Masataka Majima |
| author_sort | Makoto Katori |
| collection | DOAJ |
| description | Abstract.: It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (KATP) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as KATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs. Keywords:: salt-sensitivity, kallikrein, potassium, African-American, ebelactone B |
| first_indexed | 2024-12-22T04:12:42Z |
| format | Article |
| id | doaj.art-779118c761b5470e977e4f3af23b1a70 |
| institution | Directory Open Access Journal |
| issn | 1347-8613 |
| language | English |
| last_indexed | 2024-12-22T04:12:42Z |
| publishDate | 2006-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Pharmacological Sciences |
| spelling | doaj.art-779118c761b5470e977e4f3af23b1a702022-12-21T18:39:29ZengElsevierJournal of Pharmacological Sciences1347-86132006-01-011005370390A Missing Link Between a High Salt Intake and Blood Pressure IncreaseMakoto Katori0Masataka Majima1Department of Pharmacology, Kitasato University School of Medicine, Kitasato 1-15-1, Sagamihara, Kanagawa 228-8555, Japan; Corresponding author. Present address: Higashi 1-14-3, Shibuyaku, Tokyo 150-0011, Japan hy3m-ktr@asahi-net.or.jpDepartment of Pharmacology, Kitasato University School of Medicine, Kitasato 1-15-1, Sagamihara, Kanagawa 228-8555, JapanAbstract.: It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (KATP) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as KATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs. Keywords:: salt-sensitivity, kallikrein, potassium, African-American, ebelactone Bhttp://www.sciencedirect.com/science/article/pii/S1347861319344858 |
| spellingShingle | Makoto Katori Masataka Majima A Missing Link Between a High Salt Intake and Blood Pressure Increase Journal of Pharmacological Sciences |
| title | A Missing Link Between a High Salt Intake and Blood Pressure Increase |
| title_full | A Missing Link Between a High Salt Intake and Blood Pressure Increase |
| title_fullStr | A Missing Link Between a High Salt Intake and Blood Pressure Increase |
| title_full_unstemmed | A Missing Link Between a High Salt Intake and Blood Pressure Increase |
| title_short | A Missing Link Between a High Salt Intake and Blood Pressure Increase |
| title_sort | missing link between a high salt intake and blood pressure increase |
| url | http://www.sciencedirect.com/science/article/pii/S1347861319344858 |
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